The relationships between hyperthermia, dehydration and oxidative stress have been thoroughly studied separately within the literature both in vitro and in vivo. However, no in vivo attempts have been made to manipulate the hydration status of individuals to investigate the resulting changes in oxidative and cellular stress during and after exercise in hyperthermic conditions and what effect these changes may have on exercise performance. The purpose of the first experiment was to investigate the effects of exercise-induced dehydration with and without hyperthermia on oxidative stress. Seven healthy male trained cyclists (mean ± SD) age: 36 ± 6 yrs, height: 177.4 ± 6.5 cm, weight: 72.8 ± 7.0 kg, and power output (PO) at lactate threshold (LT): 199.3 ± 19.0 Watts (W) completed 90 min cycling exercise at 95% LT followed by a 5 km time trial (TT) in four conditions: 1) euhydration in a warm environment (EU-W, control), 2) dehydration in a warm environment (DE-W), 3) euhydration in a thermoneutral environment (EU-T), and 4) dehydration in a thermoneutral environment (DE-T) (W: 33.9 ± 0.9°C; T: 23.0 ± 1.0°C). Whole blood oxidised glutathione (GSSG) increased significantly post exercise in dehydration trials only (DE-W: p < 0.01, DE-T: p = 0.03), and while not significant, whole blood total glutathione (TGSH) and plasma thiobarbituric acid reactive substances (TBARS) tended to increase post exercise in dehydration trials (p = 0.08 for both). Intracellular monocyte heat shock protein 72 (HSP72) concentration was increased (p = 0.01) while intracellular lymphocyte HSP32 concentration was decreased for all trials (p = 0.02). Exercise-induced dehydration led to an increase in GSSG concentration while maintenance of euhydration attenuated these increases regardless of environmental condition. Additionally, evidence of increased cellular stress (measured via HSP) was found during all trials independent of body mass loss and environment. Finally, total distance covered during 90 min and PO during both 90 min and 5 km TT performance were reduced during only the DE-W trial, likely a result of combined cellular stress, hyperthermia and dehydration. These findings highlight the importance of fluid consumption during exercise to attenuate thermal and oxidative stress during prolonged exercise in the heat. The purpose of the second experiment was to investigate the effect of prolonged exercise-induced dehydration with and without hyperthermia on cellular and oxidative stress markers in untrained individuals, to serve as a comparison to the results of the first experimental chapter. Seven untrained male university students (mean ± SD) age: 21 ± 3 yrs, height: 181.1 ± 9.2 cm, weight: 76.8 ± 8.8 kg, and PO at LT 100.0 ± 13.0 W, who were unacclimatised to heat, participated in this study. Subjects completed the same experimental protocol as outlined in experimental chapter one, in warm (33.9 ± 1.0°C) and thermoneutral (22.9 ± 1.0°C) environments. Whole blood GSSG increased an average of 32% (p < 0.01) as a result of prolonged exercise, however unlike the trained subjects of experiment one, there was no effect of body mass loss on GSSG (p = 0.63). Similarly, intracellular monocyte HSP72 concentration increased 14% (p < 0.01) as a result of prolonged cycling regardless of body mass loss and environmental heat stress, analogous to subjects in experiment one. While there were no significant changes as a result of hydration or environment, a relationship was found between GSSG concentration and body mass loss (r2 = 0.5, p = 0.05), while HSP72 was correlated with body temperature and levels of heat storage (r2 = 0.5, p = 0.01). Similar to the trained individuals in experiment one, PO during the 90 min (7%, p < 0.01) and TT (14%, p < 0.01) were decreased while thermoregulation was impaired during DE-W only. These results demonstrate the increased level of stress in untrained subjects as a result of exercise and highlight the importance of participation in recommended physical activity to aid in positive cellular adaptations leading to superior antioxidant defences to aid in disease prevention. In light of the findings from the first experimental chapter that dehydration can significantly influence oxidative stress in trained subjects, the purpose of the third experimental chapter was to compare pre-exercise hyperhydration with plain water (W) or water with glycerol (G) to no hyperhydration (C) on markers of oxidative stress prior to and after a 90 min TT. Seven trained male cyclists and triathletes (age: 28 ± 8 yrs, height: 178.4 ± 7.8 cm, and mass: 73.2 ± 9.6 kg) covered as much distance as possible during a 90 min cycle after G, W or C. Blood was collected pre ingestion (PRE), post ingestion/pre exercise (PI), immediately post exercise (PE) and 1 hour post exercise (1HR) and analysed for whole blood TGSH, GSSG, and plasma levels of lipid hydroperoxides (LOOH) and protein carbonyls (PC). TGSH concentration increased post exercise in W and C (p < 0.01) while PC concentration increased post exercise during C only (p = 0.03). Additionally, GSSG concentration was greater PI and PE in C compared to G (p = 0.05, and p < 0.01, respectively), likely due to the inferior amount of fluid retained during C compared to the G and W trials. Therefore, it appears that both pre exercise hyperhydration with ad libitum fluid ingestion during exercise is sufficient to attenuate rises in exercise-induced oxidative stress. The novel findings presented in this thesis indicate fluid ingestion plays a vital role in providing cellular protection from oxidative stress. These results suggest that individuals participating in prolonged exercise should consume adequate fluid during exercise to avoid dehydration, matching fluid intake with body mass loss. Additionally, individuals who wish to hyperhydrate prior to exercise may enhance their ability to delay dehydration and thus enhance their cellular protection from oxidative stress.

Hamstring strains are one of the primary injuries within modern soccer match-play. The injury is well recognised by medical personnel, coaches and athletes as a major concern causing significant financial costs and lost time from training and matches. The temporal pattern of hamstring injury incidence during matches has shown almost half of all injuries to occur during the latter stages of each half, thus suggesting fatigue as an important contributing factor for injury. This thesis comprises four experimental chapters that examine the effect of multidirectional soccer-specific fatigue on the primary aetiological risk factors and mechanism of injury. This was then used to create and evaluate an injury prevention programme aimed at reducing the risk of hamstring strains in soccer.

Thesis (Ed. D.)--West Virginia University, 2000. / Title from document title page. Document formatted into pages; contains viii, 126 p. : ill. Includes abstract. Includes bibliographical references (p. 74-85).

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2009. / Title from title screen (site viewed February 25, 2010). PDF text: vii, 174 p. ; 2 Mb. UMI publication number: AAT 3386757. Includes bibliographical references. Also available in microfilm and microfiche formats.

Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 143-152).

Thesis (Ph.D.) - James Cook University, 2007. / Typescript (photocopy) Bibliography: leaves 213-270.

Thesis (M.S.)--University of Michigan, 1989. / eContent provider-neutral record in process. Description based on print version record.

Thesis (M.S.)--University of Michigan, 1989.

Thesis (Ph. D.)--Texas State University--San Marcos, 2009. / Vita. Includes bibliographic references (leaves 46-50, 89-94, 128-132). Also available on microfilm.

Title from title page of PDF (University of Missouri--St. Louis, viewed April 5, 2010). Includes bibliographical references (p. 119-141).